Wojciech Kozubski

Poznan University of Medical Sciences, Posen, Greater Poland Voivodeship, Poland

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Publications (115)167.72 Total impact

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    ABSTRACT: Despite the growing body of literature on the consequences of providing non-professional care to stroke survivors, the determinants of caregiving burden are still not fully recognized. Identification of significant determinants can facilitate caregiver intervention programs. The aim of this study was to evaluate the level of burden borne by caregivers of stroke patients and to identify the most important determinants of burden at 6 months after hospitalization.
    Archives of Medical Science 10/2014; 10(5):941-50. · 1.89 Impact Factor
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    ABSTRACT: Polimorfizm promotora genu G-308A TNFα a ryzyko udaru niedokrwiennego. Czynnik martwicy nowotworu alfa (TNFα) jest ważnym mediatorem immunologicznym i może współdziałać w zapoczątkowaniu i postępie udaru niedokrwiennego. Genetyka cząsteczki TNFα może mieć ważną rolę w ryzyku udaru. Najbardziej interesujący aspekt polimorfizmu G-308 A pozostaje niewyjaśniony, z powodu wielu różnic w wynikach badań. Różnice etniczne w badanych kohortach mogą stanowić jedną z przyczyn wystąpienia udaru niedokrwiennego. Nasz badany materiał dotyczył 101 chorych z udarem niedokrwiennym, w tym 30% zdiagnozowano jako udar lakunarny. Rozpoznanie było oparte na nagłym występowaniu objawów neurologicznych, trwających dłużej niż 24 godziny i potwierdzonych przez metody neuroobrazowania. Wszyscy badani byli Polakami rasy kaukaskiej. 100 przypadkowo wybranych osób bez objawów choroby naczyniowej ośrodkowego układu nerwowego stanowiło materiał kontrolny. Częstość występowania polimorfizmu G-308A genu TNFα była określana jak opisano przez Rubattu i wsp. /2005/ [11]. Rozdział genotypów w naszym materiale był podobny i nieistotny statystycznie pomiędzy chorymi i grupą kontrolną. Heterozygoty G/A były stwierdzone u 9% chorych i w 15% przypadków grupy kontrolnej, homozygoty A/A były stwierdzone u 5% chorych i tylko u 1 osoby kontrolnej, a G/G u 87% chorych i u 84% osobników kontrolnych. Nasze wyniki są więc negatywne odnośnie możliwego znaczenia polimorfizmu G-308A TNFα w ryzyku udaru niedokrwiennego u osób rasy kaukaskiej, żyjących w Polsce.
    Neurologia i neurochirurgia polska 10/2014; · 0.54 Impact Factor
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    ABSTRACT: Despite a significant progress in prevention, treatment and management in the past decades, stroke remains the most common disabling chronic condition in adult population. It may be a source of serious temporary or permanent consequences. These consequences should be recognised and measured for defining and implementation of remedial interventions and for optimum utilisation of health care resources. The aim of this work was to present sequels of stroke, taking into account objective and subjective indices, as documented in the recent literature of the subject. Selected data on mortality and survival following stroke were presented, the up-to-date literature was reviewed and register-based prospective studies were presented on quality of life (QoL) in post-stroke patients. Systematic reviews and meta-analyses of randomised controlled trials (RCTs) were summed up, related to efficacy of interventions aimed at improving QoL of the patients. Moreover, the studies were reviewed on burden and QoL experienced by caregivers of post-stroke patients and results were summed up of RCT synthesis aimed at reducing the burden and at improving QoL in the caregivers. The analysed studies indicated that stroke exerts a long-term, negative effect on patients’ QoL, promoting a decrease in this measure and burdening a significant proportion of the family caregivers. The applied till now different interventions and programmes targeted at the patients and at their carers analysed in RCTs showed no or modest effects on improving of QoL or reducing the caregiver's burden.
    Neurologia i neurochirurgia polska 07/2014; · 0.54 Impact Factor
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    ABSTRACT: Alzheimer’s disease (AD), a progressive neurodegenerative disorder leads to production of β‐amyloid (Aβ) which accumulation, facilitated in apolipoprotein E (APOE) ε‐4 carriers, results in brain degeneration by apoptosis, which may arise from oxidative damage generated by Aβ and checkpoint proteins deregulation, such as p53. The aim of the study was to analyze the mutation status in highly conservative exon 7 of TP53 and APOE allele, as well as p53 protein level in AD patients and control subjects. The study on TP53 and APOE was performed on 29 AD patients and 16 control subjects. The TP53 exon 7 was analyzed in DNA extracted from blood by sequencing and APOE allele was determined by RT‐PCR mismatchprimer technique. The p53 protein level was determined in peripheral lymphocytes by Western Blotting. The sequencing of exon 7 of TP53 revealed the presence of two various mutations only in AD patients: a missense mutation C748A (P250T, 3.4%) present in an APOE ε‐3/ε‐4 allele carrier and a silent mutation C708T (Y236Y), found in 6 (20.1%) AD patients with various APOE genotypes (ε‐2/ε‐3, ε‐3/ε‐3 and ε‐3/ε‐4). The analysis of APOE showed ε‐3/ε‐3 genotype to be more common in control group (62.5%) than in AD patients (37.9%). The ε‐3/ε‐4 variant was more abundant in AD group (44.8%) as compared to controls (31.3%). Variant ε‐4/ε‐4 occurred in a single AD patient, whereas ε‐2/ε‐2 genotype was found only in a control subject. Our results indicated that in the AD group the p53 level was highest in APOE ε‐4 carriers and did not change significantly in control group. It is most likely that both: mutations in the TP53 gene and APOE status participate in the pathogenesis of AD.
    ApoE, ApoE Receptors & Neurodegeneration Symposium; 06/2014
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    ABSTRACT: Neurodegeneration with brain iron accumulation (NBIA) defines a heterogeneous group of progressive neurodegenerative disorders characterized by excessive iron accumulation in the brain, particularly affecting the basal ganglia. In the recent years considerable development in the field of neurodegenerative disorders has been observed. Novel genetic methods such as autozygosity mapping have recently identified several genetic causes of NBIA. Our knowledge about clinical spectrum has broadened and we are now more aware of an overlap between the different NBIA disorders as well as with other diseases. Neuropathologic point of view has also been changed. It has been postulated that pantothenate kinase-associated neurodegeneration (PKAN) is not synucleinopathy. However, exact pathologic mechanism of NBIA remains unknown. The situation implicates a development of new therapies, which still are symptomatic and often unsatisfactory. In the present review, some of the main clinical presentations, investigational findings and therapeutic results of the different NBIA disorders will be presented.
    Neurologia i neurochirurgia polska 05/2014; 48(3):206-213. · 0.54 Impact Factor
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    ABSTRACT: Hyperhomocysteinemia is a well-known cardiovascular risk factor and its elevation is established in overt hypothyroidism. Since some authors suggest that chronic autoimmune thyroiditis per se may be considered as a novel risk factor of atherosclerosis independent of thyroid function, the analysis of classical cardiovascular risk factors might be helpful in evaluation the causative relationship. Data concerning the impact of thyroid autoimmunity in euthyroid state on homocysteine (Hcy) level is lacking. The aim of this study was to evaluate Hcy level in context of anti-thyroperoxidase antibodies (TPOAbs) in euthyroidism. It is a case-control study. 31 euthyroid women treated with levothyroxine (L-T4) due to Hashimoto thyroiditis (HT) and 26 females in euthyroidism without L-T4 replacement therapy were enrolled in the study. All women with HT had positive TPOAbs. Forty healthy females negative for TPOAbs comparable for age and body mass index (BMI) participated in the study as controls. Exclusion criteria were a history of any acute or chronic disease, use of any medications (including oral contraceptives and vitamin supplements), smoking, alcoholism. TPOAbs titers were higher in both groups of HT patients versus the healthy controls. Hcy levels were found to be significantly lower in treated HT patients (Me 11 mumol; IQR 4.2 mumol) as compared with healthy controls (Me 13.35 mumol; IQR 6.34 mumol; p = 0.0179). In contrast, no significant difference was found between non treated HT and control group in Hcy level. The study groups and the controls did not differ in age and BMI. Furthermore, levels of TSH, FT4, TC, LDL, HDL and TAG did not differ between the study group and the control group. The main finding of the study is a decrease in Hcy level in treated HT as compared with healthy controls. Based on our observations one can also assume that correct L-T4 replacement was associated here with a decrease of Hcy. Furthermore, it seems that non treated HT in euthyroidism is not associated with Hcy increase, in contrast to overt hypothyroidism. This may be just another argument against the concepts about the role of "euthyroid HT" in the development of atherosclerosis.
    BMC Endocrine Disorders 03/2014; 14(1):18. · 1.67 Impact Factor
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    Piotr Iwanowski, Wojciech Kozubski, Jacek Losy
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    ABSTRACT: Nummular headache (NH) is a rarely recognized primary headache, the diagnostic criteria of which are contained in the appendix to the 2nd edition of the International Classification of Headache Disorders (code A13.7.1). We present the case of a 61-year-old female who suffers, regardless of NH, from right-sided occipital neuralgia. The applied treatment - gabapentin and mianserin - had no effect. Injection of bupivacaine twice to the right occipital region resulted in neuralgia resolution up to three months, with no effect on NH. This confirms the independence of two abovementioned head pain conditions.
    Neurologia i neurochirurgia polska 03/2014; 48(2):141-3. · 0.54 Impact Factor
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    ABSTRACT: Parkinson's disease (PD) is one of the most common neurological diseases in elderly people. The mean age of onset is 55 years of age, and the risk for developing PD increases 5-fold by the age of 70. In PD, there is impairment in both motor and nonmotor (NMS) functions. The strategy of PD motor dysfunction treatment is simple and generally based on the enhancement of dopaminergic transmission by means of the L-dihydroxyphenylalanine (L-dopa) and dopamine (DA) agonists. L-dopa was discovered in the early -60's of the last century by Hornykiewicz and used for the treatment of patients with PD. L-dopa treatment in PD is related to decreased levels of the neurotransmitter (DA) in striatum and ab-sence of DA transporters on the nerve terminals in the brain. L-dopa may also indirectly stimulate the receptors of the D1 and D2 families. Administration of L-dopa to PD patients, especially long-time therapy, may cause side effects in the form of increased toxicity and inflammatory response, as well as disturbances in biothiols metabolism. Therefore, in PD pa-tients treated with L-dopa, monitoring of oxidative stress markers (8-oxo-2'-deoxyguanosine, apoptotic proteins) and in-flammatory factors (high-sensitivity C-reactive protein, soluble intracellular adhesion molecule), as well as biothiol com-pounds (homocysteine, cysteine, glutathione) is recommended. Administration of vitamins B6, B12, and folates along with an effective therapy with antioxidants and/or anti-inflammatory drugs at an early stage of PD might contribute to improvement in the quality of the life of patients with PD and to slowing down or stopping the progression of the disease.
    Current Genomics 02/2014; 15(1):11-7. · 2.87 Impact Factor
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    ABSTRACT: Knowledge on the genetics of movement disorders has advanced significantly in recent years. It is now recognized that disorders of the basal ganglia have genetic basis and it is suggested that molecular genetic data will provide clues to the pathophysiology of normal and abnormal motor control. Progress in molecular genetic studies, leading to the detection of genetic mutations and loci, has contributed to the understanding of mechanisms of neurodegeneration and has helped clarify the pathogenesis of some neurodegenerative diseases. Molecular studies have also found application in the diagnosis of neurodegenerative diseases, increasing the range of genetic counseling and enabling a more accurate diagno-sis. It seems that understanding pathogenic processes and the significant role of genetics has led to many experiments that may in the future will result in more effective treatment of such diseases as Parkinson's or Huntington's. Currently used molecular diagnostics based on DNA analysis can identify 9 neurodegenerative diseases, including spinal cerebellar ataxia inherited in an autosomal dominant manner, dentate-rubro-pallido-luysian atrophy, Friedreich's disease, ataxia with ocu-lomotorapraxia, Huntington's disease, dystonia type 1, Wilson's disease, and some cases of Parkinson's disease.
    Current Genomics 02/2014; 15(1):18-27. · 2.87 Impact Factor
  • Anna Oczkowska, Wojciech Kozubski, Jolanta Dorszewska
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    ABSTRACT: Parkinson's disease (PD) is a degenerative disease of the central nervous system, of which patomechanizm entirely is not clear. In the picture neuropathologically there is observed degeneration and loss of dopaminergic neurons, but also noradrenergic, serotonergic and cholinergic neurons in patients with PD. It is believed, that causes of PD are both environmental and genetic factors, associated mainly with mutations in the SNCA and PRKN genes, which may lead to changes in the structure of proteins such as alpha-synuclein (ASN) and Parkin. In neurons, disorders of the protein structure can lead to its aggregation and formation of soluble oligomers and insoluble filaments in the form of Lewy bodies and Lewy neuritis. In PD aggregation of ASN can be modulated by many factors like: oxidative stress, other neuronal proteins, Parkin, catecholamines especially dopamine, and mutations of SNCA gene. It also appears that some impact on the aggregation of ASN may have destabilizing factors of ASN tetramers. That, does ASN may become a new point for pharmacotherapy in PD.
    Przegla̧d lekarski 01/2014; 71(1):26-32.
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    ABSTRACT: Alzheimer's disease (AD) leads to generation of β-amyloid (Aβ) in the brain. Alzheimer's disease model PS/APP mice show a markedly accelerated accumulation of Aβ, which may lead to apoptosis induction e.g. in cells expressing wild-type p53. The TP53 gene is found to be the most frequently mutated gene in human tumour cells. There is accumulating evidence pointing out to the contribution of oxidative stress and chronic inflammation in both AD and cancer. The purpose of this study was to analyze exon 7 mutations of the murine Trp53 gene and Aβ/A4 and p53 protein levels in PS/APP and control mice. The studies were performed on female double transgenic PS/APP mice and young adults (8-12 weeks old) and age-matched control mice. The Trp53 mutation analysis was carried out with the use of PCR and DNA sequencing. The Aβ/A4 and p53 levels were analyzed by Western blotting. The frequency of mutations was almost quadrupled in PS/APP mice (44%), compared to controls (14%). PS/APP mice with the A929T and A857G mutations had a similar p53 level. In cerebral gray matter of PS/APP mice the level of p53 positive correlated with the level of Aβ protein (RS = +0.700, p < 0.05). In younger control animals, the T854G mutation was related to p53 down-regulation, while in aging ones, G859A substitution was most likely associated with over-expression of p53. In silico protein analysis revealed a possibly substantial impact of all four mutations on p53 activity. Three mutations were in close proximity to zinc-coordinating cysteine residues. It seems that in PS/APP mice missense Trp53 exon 7 mutations may be associated with the degenerative process by changes of p53 protein function.
    Folia neuropathologica / Association of Polish Neuropathologists and Medical Research Centre, Polish Academy of Sciences. 01/2014; 52(1):30-40.
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    ABSTRACT: An elevated concentration of total homocysteine (tHcy) in plasma and cerebrospinal fluid is considered to be a risk factor for Alzheimer's disease (AD) and Parkinson's disease (PD). Homocysteine (Hcy) levels are influenced by folate concentrations and numerous genetic factors through the folate cycle, however, their role in the pathogenesis of PD remains controversial. Hcy exerts a neurotoxic action and may participate in the mechanisms of neurodegeneration, such as excitotoxicity, oxidative stress, calcium accumulation, and apoptosis. Elevated Hcy levels can lead to prooxidative activity, most probably through direct interaction with N-methyl-D-aspartate (NMDA) receptors and sensitization of dopaminergic neurons to age-related dysfunction and death. Several studies have shown that higher concentration of Hcy in PD is related to long-term administration of levodopa (L-dopa). An elevation of plasma tHcy levels can also reflect deficiencies of cofactors in remethylation of Hcy to methionine (Met) (folates and vitamin B12) and in its transsulfuration to cysteine (Cys) (vitamin B6). It is believed that the increase in the concentration of Hcy in PD can affect genetic polymorphisms of the folate metabolic pathway genes, such as MTHFR (C677T, A1298C and G1793A), MTR (A2756G), and MTHFD1 (G1958A), whose frequencies tend to increase in PD patients, as well as the reduced concentration of B vitamins. In PD, increased levels of Hcy may lead to dementia, depression and progression of the disease.
    Current Genomics 12/2013; 14(8):534-42. · 2.87 Impact Factor
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    ABSTRACT: Although Parkinson's disease (PD) was first described almost 200 years ago, it remains an incurable disease with a cause that is not fully understood. Nowadays it is known that disturbances in the structure of pathological proteins in PD can be caused by more than environmental and genetic factors. Despite numerous debates and controversies in the literature about the role of mutations in the SNCA and PRKN genes in the pathogenesis of PD, it is evident that these genes play a key role in maintaining dopamine (DA) neuronal homeostasis and that the dysfunction of this homeostasis is relevant to both familial (FPD) and sporadic (SPD) PD with different onset. In recent years, the importance of alphasynuclein (ASN) in the process of neurodegeneration and neuroprotective function of the Parkin is becoming better understood. Moreover, there have been an increasing number of recent reports indicating the importance of the interaction between these proteins and their encoding genes. Among others interactions, it is suggested that even heterozygous substitution in the PRKN gene in the presence of the variants +2/+2 or +2/+3 of NACP-Rep1 in the SNCA promoter, may increase the risk of PD manifestation, which is probably due to ineffective elimination of over-expressed ASN by the mutated Parkin protein. Finally, it seems that genetic testing may be an important part of diagnostics in patients with PD and may improve the prognostic process in the course of PD. However, only full knowledge of the mechanism of the interaction between the genes associated with the pathogenesis of PD is likely to help explain the currently unknown pathways of selective damage to dopaminergic neurons in the course of PD.
    Current Genomics 12/2013; 14(8):502-17. · 2.87 Impact Factor
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    ABSTRACT: Epinephrine (E) and sympathetic nerve stimulation were described by Thomas Renton Elliott in 1905 for the first time. Dopamine (DA), norepinephrine (NE), E, and serotonin (5-HT) belong to the classic biogenic amines (or monoamines). Parkinson's disease (PD) is among the diseases in which it has been established that catecholamines may account for the neurodegeneration of central and peripheral catecholamine neural systems. PD is a chronic and progressive neurological disorder characterized by resting tremor, rigidity, and bradykinesia, affecting 2% of individuals above the age of 65 years. This disorder is a result of degeneration of DA-producing neurons of the substantia nigra and a significant loss of noradrenergic neurons in the locus coeruleus. In PD and other related neurodegerative diseases, catecholamines play the role of endogenous neurotoxins. Catechol-O-methyltransferase (COMT) and/or monoamine oxidase (MAO) catalyze the metabolism of monoamines. However, the monoamine transporters for DA, NE, and 5-HT namely DAT, NET, and SERT, respectively regulate the monoamine concentration. The metabolism of catecholamines and 5-HT involves common factors. Monoamine transporters represent targets for many pharmacological agents that affect brain function, including psychostimulators and antidepressants. In PD, polymorphisms of the COMT, MAO, DAT, NET, and 5- HTT genes may change the levels of biogenic amines and their metabolic products. The currently available therapies for PD improve the symptoms but do not halt the progression of the disease. The most effective treatment for PD patients is therapy with L-dopa. Combined therapy for PD involves a DA agonist and decarboxylase, MAOs and COMT inhibitors, and is the current optimal form of PD treatment maintaining monoamine balance.
    Current Genomics 12/2013; 14(8):518-33. · 2.87 Impact Factor
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    ABSTRACT: Lung cancer is recognized among the most frequent causes of paraneoplastic neurological syndromes (PNS). Neurological syndromes in subjects with systemic malignancy remain a clinical and diagnostic challenge. The aim of the study was to evaluate the frequency of NPS, their clinical manifestation and association with onconeural antibodies in patients with lung cancer. Fifty patients hospitalized with the diagnosis of PNS participated in the study. Neurological evaluation consisted of the Rankin scale (mRS), the Barthel index (BI), and testing for the presence of onconeural antibodies by means of indirect immunofluorescence, as screening, and Western blotting as confirmation. The majority of lung cancer patients (64%) aged 62 ± 10 had NPS symptoms. Their neurological condition and daily living activities were reasonable: mRS (1.0; 0.0-4.0) and BI (100; 7.4-100) scores. Classical PNS were found in 30% of cases and included sensory neuropathy (16%), paraneoplastic cerebellar degeneration (12%) as the most frequent symptoms. Autoimmune reaction was observed in 42% of lung cancer patients and in 20% was represented by well-characterized onconeural antibodies. Anti-Hu antibody was identified as the most frequent. In conclusion, PNS signs in lung cancer patients have both classical and non-classical features. In the course of SCLC only well-characterized onconeural antibodies were identified. The presence of well-characterized onconeural antibodies is strongly associated with classical features of PNS.
    Advances in Experimental Medicine and Biology 01/2013; 756:333-9. · 2.01 Impact Factor
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    ABSTRACT: Leptin is an adipokine that in vitro enhances agonist-induced platelet aggregation and adipokine expression. Hyperleptinaemia represents a risk factor for cardiovascular disease. We conducted a prospective evaluation of the potential link between blood platelet activation and plasma leptin levels in post-stroke patients. Using five-colour flow cytometry, the platelet surface expression of CD40L, CD62P, the subpopulations of monocyte-platelet aggregates and platelet-derived microparticles (PMPs) as well as the plasma leptin, soluble leptin receptor (sOb-R), leptin/sOb-R ratio, the plasma adiponectin, and leptin/adiponectin ratio were assessed in 98 stroke patients on the first (V₀), 10th (V₁ ) and 90th (V₂) day after stroke and once in 78 age-, gender- and vascular risk factor-matched disease controls. We demonstrated that at V0 leptin resistance, defined as leptin/sOb-R ratio, was higher than in the controls [1.1 (0.5-1.8 vs. 0.5 (0.2-1.1); p=0.02]. After adjustment according to the factors which influence platelet activation, we confirmed the relationship between percentage of circulating PMPs and plasma leptin level (B=0.18; p=0.02) or the leptin/sOb-R ratio (B=0.23; p=0.02) in normal-weight subjects in the acute phase of stroke. No correlation could be demonstrated between the adipokine parameters and the percentage of monocyte-platelet aggregates or expression of platelet pro-inflammatory glycoproteins. In conclusion, formation of PMPs on the first day following an ischaemic stroke shows a positive correlation with leptin levels and with resistance to leptin. Leptin level does not seem to affect the expression of platelet surface proinflammatory glycoproteins.
    Thrombosis and Haemostasis 05/2012; 108(1):107-18. · 5.76 Impact Factor
  • Neurology 04/2012; 78(Meeting Abstracts 1):P06.007-P06.007. · 8.30 Impact Factor
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    Wojciech Kozubski
    Polskie archiwum medycyny wewnȩtrznej 03/2012; 122(3):125-6. · 2.05 Impact Factor
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    ABSTRACT: Platelets participate in the development and progression of atherosclerosis. During this process they interact with endothelial cells and leukocytes. Therefore, we investigated the associations between carotid atherosclerosis and platelet reactivity markers. The platelet surface expression of P-selectin (CD62P) and the activated GPIIb/IIIa receptor (corresponding to increased binding of PAC-1), as well as the fraction of platelet-derived microparticles (PMPs) prior to and after platelet stimulation with TRAP or ADP, were determined using flow cytometry in 94 subjects in the convalescent phase of ischaemic stroke and in 76 disease controls. The mean common carotid intima-media thickness (CCA(mean) IMT), maximal common carotid IMT (CCA(max) IMT) and maximal bifurcation IMT (BIF(max) IMT) were measured bilaterally using B mode, colour Doppler ultrasonography. In stroke subjects IMT within CCA and BIF were greater than in disease controls and the percentage of PMPs prior to and after ex vivo stimulation with agonists was significantly higher than in controls. Multiple regression analysis revealed that PMPs were positively and independently correlated with both CCA(mean) IMT ( β = 0.23; p < 0.01) and stroke ( β = 0.21; p<0.01), while PAC-1 binding to platelets activated with ADP was negatively and independently associated with CCA(mean) IMT ( β = -0.29; p<0.001) and atherosclerotic carotid plaque presence ( β = -0.28, p = 0.003). We found a positive association between enhanced PMP formation and atherosclerotic thickening of carotid intima-media or carotid plaque in patients after ischaemic stroke. We demonstrated that diminished expression of active GPIIb/IIIa in the ADP-activated platelets is associated with increased carotid IMT, independently of stroke.
    Platelets 02/2012; · 2.63 Impact Factor
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    ABSTRACT: The white blood cell count and mean platelet volume determined shortly after the symptom onset are known as independent predictors for clinical outcome after stroke. In the present study we sought to evaluate the prognostic value of platelet-derived inflammatory biomarkers measured prospectively after an ischaemic event. Using five-colour flow cytometry, the platelet surface expression of CD40L, CD62P and subpopulations of leukocyte-platelet aggregates were assessed in 93 stroke patients on the first (V(0)), 10th (V(1)) and 90th (V(2)) day after stroke, and once in 65 disease controls. The clinical outcome was evaluated using the Scandinavian Stroke Scale (SSS) and modified Rankin Scale (mRS) at the same time points as blood sampling and 24 months after the event. Patients with either CD40L surface expression or the percentage of monocyte-platelet aggregates (M-plt) in the third tertile (T3) at V0 had a significantly lower score on the SSS at V(1). Patients with the percentage M-plt at V(0) higher than the median value of M-plt in controls were at increased risk of SSS < 40 at V(1) (odds ratio: 2.6; 95% confidence interval [CI]: 1.4 - 8.7; p=0.006). Patients with the percentage of M-plt in T3 at V(0) showed progressive decline in survival (hazard ratio [HR]: 1.6; 95% CI: 1.1-1.9; p=0.02) and a significantly higher number of recurrent vascular events (HR: 2.64; 95% CI: 1.3-3.2; p=0.02) when compared to the first tertile. In conclusion, increased levels of M-plt could be a predictive marker for both early outcome and long-term prognosis while increased CD40L was correlated with worse clinical outcome.
    Thrombosis and Haemostasis 02/2012; 107(2):346-55. · 5.76 Impact Factor

Publication Stats

374 Citations
167.72 Total Impact Points

Institutions

  • 1999–2014
    • Poznan University of Medical Sciences
      • Department of Neurology
      Posen, Greater Poland Voivodeship, Poland
  • 2009–2012
    • Uniwersytet Medyczny im.Karola Marcinkowskiego w Poznaniu
      Posen, Greater Poland Voivodeship, Poland
  • 2004
    • Polish Academy of Sciences
      • Institute of Human Genetics
      Warsaw, Masovian Voivodeship, Poland
  • 2003
    • Poznańskie Centrum Superkomputerowo-Sieciowe
      Posen, Greater Poland Voivodeship, Poland